A number of studies have recently used modern neuropsychological techniques to investigate abnormalities in impulsive personality disorders. In the lead editorial in this issue, Rogers (pp. 1335–1340) reviews this growing field.

There has been revived interest within the last few years in neuropsychological investigations of personality disorders (PDs) associated with impulsive and/or anti-social behaviour. Neuropsychological studies of such PDs offer two potential benefits: (i) an improving characterization of the cognitive and emotional difficulties experienced by individuals diagnosed with these disorders and, in particular, borderline PD and anti-social PD; (ii) the development of more precise hypotheses about the role of brain dysfunction in the aetiology and behavioural problems associated with these conditions. The most recent neuropsychological studies of impulsive PD have been interpreted against a background of accumulating evidence for structural (Driessen et al. 2000; Raine et al. 2000; Dolan et al. 2001), neurochemical (Coccaro & Siever, 1995; Steinberg et al. 1997; Leyton et al. 2001) and functional brain abnormalities (Donegan et al. 2003). Future studies of impulsive PDs will be able to exploit advances in structural imaging (e.g. diffusion tensor imaging/tract mapping, e.g. Hoptman et al. 2002), as well as pharmacological and behavioural genetics (McGuffin & Thapar, 1992; Lesch et al. 1996; Skodol et al. 2002).

Background. Childhood adversity significantly increases the risk of depression, but it is unclear whether this risk is most pronounced for depression occurring early in life. In the present study, we examine whether three aspects of childhood adversity – low socio-economic status (SES), family disruption, and residential instability – are related to increased risk of depression during specific stages of the life course. We also examine whether these aspects of childhood adversity are related to the severity of depression.

Method. A sample of 1089 of the 4140 births enrolled in the Providence, Rhode Island cohort of the National Collaborative Perinatal Project was interviewed between the ages of 18 and 39. Measures of parental SES, childhood family disruption and residential instability were obtained upon mother's enrolment and at age 7. Age at onset of major depressive episode, lifetime number of depressive episodes, and age at last episode were ascertained via structured diagnostic interviews. Survival analysis was used to identify risk factors for depression onset and remission and Poisson regression was used to model the recurrence rate of depressive episodes.

Results. Low parental SES, family disruption and a high level of residential instability, defined as three or more family moves, were related to elevated lifetime risks of depression; the effects of family disruption and residential instability were most pronounced on depression onset by age 14. Childhood adversity was also related to increased risk of recurrence and reduced likelihood of remission.

Conclusions. Childhood social disadvantage significantly influences risk of depression onset both in childhood and in adulthood. Early childhood adversity is also related to poor prognosis.

Background. The aim of this paper was to examine the association between major depression and cigarette smoking among young adults in a birth cohort before and after adjusting for confounding factors.

Method. Data were gathered over the course of the Christchurch Health and Development Study (CHDS). The CHDS is a longitudinal study of a birth cohort of 1265 New Zealand children studied to age 21. Data were gathered by interview on: (a) major depression over the period 16–21 years; (b) daily smoking and nicotine dependence over the period from 16–21 years. In addition, the study included extensive information on social, family, and behavioural factors in childhood and adolescence.

Results. Young people meeting DSM-IV criteria for major depression had elevated rates of daily smoking and nicotine dependence. These associations were reduced substantially by control for potential confounding child and adolescent factors. Nonetheless, even after such control, major depression was associated with increased rates of daily smoking (IRR=1·19; 95% CI=1·03, 1·39) and elevated rates of nicotine dependence (OR=1·75; 95% CI=1·13, 2·70).

Conclusions. The results suggest that much of the association between smoking and depression reflects common confounding factors that are associated with both outcomes. Nonetheless, even after control for these factors there is evidence of a possible causal linkage between smoking and depression. The direction of causality between smoking and depression remains unknown.

Background. This paper examines the associations between puberty and three important health behaviours (smoking, food intake and exercise) and explores whether these associations are mediated by puberty's relationship to stress and psychological difficulties.

Method. Data were taken from the first year of the ongoing, 5-year, Health and Behaviours in Teenagers Study (HABITS). This is a school-based study set in 36 schools in London. In the first year of the study, 4320 students (2578 boys, 1742 girls) in their first year of secondary education took part.

Results. Among girls, being more pubertally advanced was associated with a greater likelihood of having tried smoking. Among boys, being more pubertally advanced was associated with a greater likelihood of having tried smoking, a higher intake of high-fat food and higher levels of exercise. More pubertally advanced girls experienced more stress but not more psychological difficulties. There were no associations between puberty and either stress or psychological difficulties in boys. Stress and psychological difficulties were associated with health behaviours in girls and boys, but neither of these factors mediated the relationship between pubertal stage and health behaviours found in girls.

Conclusions. These results suggest that the onset of puberty has a marked effect on the development of health behaviours. Puberty was related to an acceleration of the development of unhealthy behaviours, except for exercise behaviour in boys, where advanced puberty was associated with more exercise. These changes were unrelated to adolescent issues of stress and a causal explanation for these associations must be sought elsewhere.

Background. Dieting in healthy women results in a decrease in the availability of tryptophan (TRP), the amino-acid precursor of serotonin (5-HT), for brain 5-HT synthesis. This is associated with increases in the prolactin response to 5-HT drug challenge suggesting a ‘supersensitivity’ of 5-HT neuroendocrine responses. The aim of the study was to assess whether increased TRP intake during dieting would prevent the changes in TRP availability and 5-HT neuroendocrine function.

Method. Fifty female subjects underwent a 1000 kcal daily diet for 3 weeks. In the final week of the diet subjects were randomly allocated to receive either nutritionally-sourced TRP (1·8 g daily) or placebo in a double-blind, parallel group, design.

Results. TRP supplementation failed to modify the dieting-induced reduction in fasting TRP availability to the brain. However, in contrast to placebo-treated subjects, subjects receiving additional TRP did not show enhanced prolactin responses to intravenous TRP challenge.

Conclusions. The decrease in TRP availability produced by dieting may be due to increased TRP metabolism rather than decreased TRP intake. While TRP treatment did not increase fasting TRP availability it may have modified the effect of dieting on brain 5-HT function. Further studies will be needed to see if this effect of TRP has consequences for the effectiveness of dieting as means of weight control.

Background. Ghrelin and leptin are endogenous peripheral proteins involved in the regulation of eating behaviour. In particular, ghrelin stimulates hunger and promotes food ingestion, whereas leptin increases satiety and reduces food consumption. Therefore, alterations in the physiology of these peptides may play a role in the pathogenesis of eating disorders such as bulimia nervosa. In the present study, we investigated ghrelin and leptin responses to food ingestion in patients with bulimia nervosa.

Method. Nine symptomatic drug-free bulimic women and 12 age-matched healthy women ingested a meal of 1207 kcal (60% carbohydrates, 23% fat and 17% proteins) at 12.00 a.m. and underwent blood sample collection before and 45, 60, 90, 120 and 180 min after the meal. Plasma levels of ghrelin, leptin, insulin and glucose were measured.

Results. In healthy women, circulating ghrelin exhibited a drastic decrease after the food intake whereas, in bulimic patients, this response was significantly blunted. No difference between the two subjects groups was observed in post-prandial profiles of plasma leptin, insulin and glucose.

Conclusions. The lack of a leptin response to food ingestion, in both bulimic and healthy women, is compatible with the role of this peptide as long-term rather than short-term modulator of eating behaviour. The blunted ghrelin response to food ingestion may support the occurrence in bulimic subjects of an impaired suppression of the drive to eat following a meal. This may have implications for binge-eating.

Background. There were four purposes of the current study, including the investigation of the: (i) adequacy of a multidimensional measure of body image; (ii) genetic and environmental epidemiology of this measure; (iii) shared variance between genetic and environmental risk factors for body mass index (BMI) and body image; and (iv) Equal Environment Assumption (EEA) as it related to body attitudes.

Method. Six types of body attitudes, as measured by the Body Attitudes Questionnaire (BAQ) and reported by 894 complete female–female twin pairs (mean age 32·35 years, S.D.=41·8) from the Australian Twin Registry, were analysed.

Results. Confirmatory factor analysis of the BAQ supported the adequacy of the measure. Additive genetic and unique environmental influences best accounted for the variance of all six of the BAQ subscales. The relationship between BMI and body attitudes was primarily due to shared genes rather than environment but the majority of genetic and environmental effects on body attitudes were independent of BMI, with the exception of the Feeling Fat subscale, which shared 53% of its genetic risk factors with BMI. One violation of the EEA was suggested, namely similarity of childhood treatment influenced similarity on Lower Body Fatness subscale.

Conclusions. Findings support the notion that: (i) body image is a multidimensional concept; (ii) it is relatively independent of BMI; and (iii) both genetic and non-shared environment are influential determinants of body attitudes.

Background. The long-term use of methamphetamine (MAMP) can result in psychosis but it is not clear why some individuals develop psychotic symptoms, while others use MAMP regularly over long periods and remain unscathed. We set out to characterize MAMP users and to examine the relationship of pre-morbid personality, pre-morbid social function and other psychiatric disorders to MAMP psychosis.

Method. Four hundred and forty-five amphetamine users were recruited from a psychiatric hospital and a detention centre in Taipei, and were assessed with the Diagnostic Interview for Genetic Studies (DIGS). Their parents were interviewed with the Premorbid Schizoid and Schizotypal Traits (PSST) and the Premorbid Social Adjustment (PSA) schedules. Pre-morbid characteristics and psychiatric co-morbidity were compared between the MAMP users with a lifetime diagnosis of MAMP psychosis and those without.

Results. The MAMP users with psychosis presented a clinical picture which mimicked the positive symptoms of schizophrenia: 85% had auditory hallucinations; 71% persecutory delusions; 63% delusions of reference. Compared with their non-psychotic counterparts, these MAMP users were younger at first MAMP use, used larger amounts of MAMP, had a significantly higher mean PSST score, and higher rates of major depressive disorder, alcohol dependence and antisocial personality disorder.

Conclusions. Earlier and larger use of MAMP was associated with increased risk of psychosis. Our data are also compatible with the view that pre-morbid schizoid/schizotypal personality predisposes MAMP users to develop psychosis, and that the greater the personality vulnerability, the longer the psychosis will persist.

Background. Although cannabis is the most widely used illicit drug in the United States, few recent American studies have examined the attributes of long-term heavy cannabis users.

Method. Using a case–control design, we obtained psychological and demographic measures on 108 individuals, age 30–55, who had smoked cannabis a mean of 18000 times and a minimum of 5000 times in their lives. We compared these heavy users to 72 age-matched control subjects who had smoked at least once, but no more than 50 times in their lives.

Results. We found no significant differences between the two groups on reported levels of income and education in their families of origin. However, the heavy users themselves reported significantly lower educational attainment (P<0·001) and income (P=0·003) than the controls, even after adjustment for a large number of potentially confounding variables. When asked to rate the subjective effects of cannabis on their cognition, memory, career, social life, physical health and mental health, large majorities of heavy users (66–90%) reported a ‘negative effect’. On several measures of quality of life, heavy users also reported significantly lower levels of satisfaction than controls.

Conclusion. Both objective and self-report measures suggest numerous negative features associated with long-term heavy cannabis use. Thus, it seems important to understand why heavy users continue to smoke regularly for years, despite acknowledging these negative effects. Such an understanding may guide the development of strategies to treat cannabis dependence.

Background. Major depressive disorder (MDD) is highly co-morbid with other Axis I disorders, which commonly precede its onset. We sought to determine the level and periods of risk for MDD posed by prior or co-occurring psychiatric disorders.

Method. Using retrospective data from a longitudinal, population-based sample of 2926 male and 1929 female adult twin subjects, we predicted the hazard rates for MDD from a Cox proportional hazards model with same-year or prior onsets of co-morbid Axis I disorders as time-dependent covariates.

Results. All axis I disorders studied (generalized anxiety disorder, panic disorder, phobia, alcohol dependence, psychoactive substance use disorders and conduct disorder) significantly predicted increased risk for developing MDD. The highest hazard rates occurred for MDD onsets that co-occurred with those of the co-morbid disorder. However, the risk for onset of MDD subsequent to that of prior disorders is also significantly increased and remains relatively unchanged over time. Although the risk for onset of MDD is significantly higher in women than men, this was not explained by gender differences in prior disorder prevalence or increased sensitivity in women to the effects of prior disorders on risk for depression.

Conclusions. Prior psychiatric disorders are significant risk factors for the development of MDD, independent of the length of the intervening period between the onset of the first disorder and that of MDD.

Background. It has been proposed that delusions of persecution are caused by the tendency to over-attribute malevolent intentions to other people's actions. One aspect of intention attribution is detecting contingencies between an agent's actions and intentions. Here, we used simplified stimuli to test the hypothesis that patients with persecutory delusions over-attribute contingency to agents' movements.

Method. Short animations were presented to three groups of subjects: (1) schizophrenic patients; (2) patients with affective disorders; and (3) normal control subjects. Patients were divided on the basis of the presence or absence of delusions of persecution. Participants watched four types of film featuring two shapes. In half the films one shape's movement was contingent on the other shape. Contingency was either ‘intentional’: one shape moved when it ‘saw’ another shape; or ‘mechanical’: one shape was launched by the other shape. Subjects were asked to rate the strength of the relationship between the movement of the shapes.

Results. Normal control subjects and patients without delusions of persecution rated the relationship between the movement of the shapes as stronger in both mechanical and intentional contingent conditions than in non-contingent conditions. In contrast, there was no significant difference between the ratings of patients with delusions of persecution for the conditions in which movement was animate. Patients with delusions of persecution perceived contingency when there was none in the animate non-contingent condition.

Conclusions. The results suggest that delusions of persecution may be associated with the over-attribution of contingency to the actions of agents.

Background. Cognitive deficits are common in major depressive disorder, but their nature is unclear. The effort hypothesis states that performance on effortful tasks is disproportionately impaired compared with the performance on automatic tasks. The cognitive speed hypothesis states that depression is characterized by cognitive slowness, which is a source of cognitive dysfunctioning. The present study investigated both theories in unmedicated adult depressive patients. It was also investigated whether the cognitive deficits can be attributed to more general physical illness-related factors or specifically to depressive disorder.

Methods. Thirty non-psychotic depressive out-patients were compared with 38 healthy control subjects and 25 patients with severe allergic rhinitis. The effects of group on more automatic and more effortful aspects of cognitive tasks measuring cognitive speed (Concept Shifting Task, Stroop Colour Word Test, Memory Scanning Test) and memory retrieval (Visual Verbal Learning Task, Verbal Fluency Test) were evaluated by MANCOVA. Age, sex, education and pre-morbid intelligence were treated as covariates.

Results. The depressive group had cognitive deficits in the automatic processing subtask of the Stroop, memory scanning and memory span. Performance on more effortful tasks was not impaired.

Conclusions. Our results are more consistent with the cognitive speed hypothesis. Cognitive functioning in depressive disorder seems to be characterized by a reduced speed of information processing in automatic subtasks.

Background. Motor function is deficient in many patients with obsessive–compulsive disorder (OCD), especially in the face. To investigate subtle motor dysfunction, kinematical analysis of emotional facial expressions can be used. Our aim was to investigate facial movements in response to humorous film stimuli in OCD patients.

Method. Kinematical analysis of facial movements was performed. Ultrasound markers at defined points of the face provided exact measurement of facial movements, while subjects watched a humorous movie (‘Mr Bean’). Thirty-four OCD patients (19 male, 15 female; mean (S.D.) age: 35·8 (11·5) years; mean (S.D.) total Y-BOCS score: 25·5 (5·9)) were studied in unmedicated state and after a 10-week treatment with the SSRI sertraline. Thirty-four healthy controls (19 male, 15 female; mean (S.D.) age: 37·5 (13·1) years) were also investigated.

Results. At baseline, OCD patients showed significantly slower velocity at the beginning of laughing than healthy controls and a reduced laughing frequency. There was a significant negative correlation between laughing frequency and severity of OCD symptoms. Ten weeks later a significant increase of laughing frequency and initial velocity during laughing was found.

Conclusions. Execution of adequate facial reactions to humour is abnormally slow in OCD patients. Susceptibility of OCD patients with regard to emotional stimuli is less pronounced than in healthy subjects. This phenomenon is closely correlated to OCD symptoms and is state-dependent.

Background. This study investigates the competence of patients with dementia, depression and schizophrenia to make treatment decisions. The outcome of an objective test instrument is presented and compared with clinical assessment of competence by the attending physician.

Method. The MacArthur Competence Assessment Tool-Treatment (MacCAT-T), a test instrument to assess abilities in different standards of competence, was administered to patients with diagnoses of dementia (N=31), depression (N=35) and schizophrenia (N=43). Statistical significance of group differences in the MacCAT-T results were tested with the chi-square test. The concordance of the test and clinical assessment of competence by the attending physician were evaluated by Cohen's kappa coefficient.

Results. Patients with dementia, as a group, showed significantly more often impaired performance than those with schizophrenia who were still more impaired than depressed patients. Patients were classified as impaired or not depending on the standards used. By combination of all standards substantially more patients were classified as impaired than by clinical assessment (67·7 v. 48·4% of patients with dementia, 20·0 v. 2·9% of patients with depression, 53·5 v. 18·4% of patients with schizophrenia).

Conclusions. Using different standards of competence the study showed substantial differences among patients with dementia, depression and schizophrenia. The high proportion of patients identified as incompetent raises several ethical questions, in particular, those referring to the selection of standards or the definition of cut-offs for incompetence. The discrepancy between clinical and formal evaluations points out the influence of the used procedure on competence judgements.

Background. A recent US study presented data suggesting that depressed women are more likely to respond to selective serotonin reuptake inhibitor (SSRI) than tricyclic (TCA) antidepressant drug therapies. We have undertaken replication studies in two independent databases.

Method. We have examined for gender differences in SSRI and TCA antidepressant response in both retrospective and prospective naturalistic uncontrolled studies, and in subsets of melancholic and non-melancholic depressed subjects. As the US study had indicated that women under the age of 40 years were particularly likely to show a differential response to SSRIs, we examined for age, gender and interactional effects. In addition, we examined for differential SSRI and TCA responsiveness in a subset of patients who had received drugs from both classes.

Results. We failed to find evidence of women having a preferential response to SSRI medication or, conversely, of men having a superior response to TCA medication. Older age, however, was associated with a superior TCA response and younger age with a superior SSRI response.

Conclusion. As few studies have examined for differential gender and age effects in response to narrow action and broad action antidepressant drugs across major depressive subtypes, gender differential effects remain to be established.

Background. Although patients with schizophrenia have increased rates of neurological soft signs, few studies have examined prospectively their trait or state characteristics in relation to psychopathology.

Method. In a prospective study of 97 patients with first-episode schizophrenia (DSM-IV criteria) we assessed neurological soft signs and psychopathology at presentation and at 6 month follow-up for 73 cases. To establish whether soft signs were associated with variations in clinical state, neurological soft signs were measured using two validated examinations (Neurological Evaluation Scale and Condensed Neurological Examination); psychopathology was assessed using the Positive and Negative Syndrome Scale.

Results. There was significant improvement in overall neurological function, primarily in motor-related and cortical signs, which were associated with improvement in psychopathology. Conversely, ‘harder’ signs were unrelated to improvement in psychopathology.

Conclusions. Neurological soft signs in schizophrenia are heterogenous. Motor and cortical signs evidence state-like characteristics and vary with clinical course, while ‘harder’ signs evidence more static, trait-like characteristics in accordance with a neurodevelopmental basis.